Fibrodysplasia ossificans progressiva is an incredibly rare disease, striking just one out of every two million people. It’s also an incredibly astonishing disease. A single mutation to a single gene causes muscles to spontaneously turn into new bones. Over time, people with fibrodysplasia ossificans progressiva (FOP for short) grow a second skeleton–one that can cut their lives short.

I wrote about FOP in “The Girl Who Turned to Bone” in the Atlantic in 2013. At the time, FOP served as a microcosm for the struggles of people with rare diseases. (In the United States, almost 30 million people have rare diseases of one kind or another.) Rare diseases have historically attracted little interest from scientists or pharmaceutical companies. Working on common diseases like cancer or diabetes seemed more likely to lead to rewards, both academic and financial. As I wrote in my article, Fred Kaplan of the University of Pennsylvania got a lot of puzzled looks from his colleagues when he decided in the late 1980s to dedicate his career to figuring out FOP. It seemed like professional suicide. And he has certainly traveled a hard road since then. It took many years for him and his colleagues to find the gene behind FOP. And then they spent many more years trying to understand how a mutation to that gene actually leads to the disease. In the meantime, Kaplan has not had any effective treatment to offer his patients with FOP.

I ended my Atlantic story on a hopeful note, observing how rare diseases like FOP were starting to gain more attention–thanks in part to the efforts of patients themselves, as well as new initiatives from the National Institutes of Health. But in the two years since the story came out, things have changed a lot faster than I would have predicted. Rare diseases are attracting a huge amount of attention, which is leading to some potential treatments. One sign of this progress is a study on FOP that’s being published today in the journal Science Translational Medicine. A team of scientists has found a molecule that appears to block the second skeleton.

The gene behind the disease, called ACVR1, encodes a molecule that sits on the surface of cells. There it can grab signaling molecules and relay messages to the interior of the cell. A team of scientists at Regeneron Pharmaceuticals engineered human cells so that they carried the mutation to ACVR1 that is found in people with FOP. Then they hurled a barrage of molecules at the cells, to see if the mutant ACVR1 responded in a peculiar way to any of them. They discovered one that triggered just such an odd response.

The molecule is called activin A. It is released by cells to help with many different tasks in the body, from the development of organs in embryos to healing wounds. The fact that activin A helps heal wounds is especially intriguing when you consider one of the most striking features of FOP: people with the disease often abruptly grow new bones after injuries–even slight ones like bumping into a table corner. Kaplan and other researchers have long wondered if the mutation that causes FOP alters the body’s ability to heal wounds. Instead of causing stem cells to rebuild muscle and other damaged tissue, the body might signal them to become bones. And activin A might carry that faulty signal. In normal cells, it silences ACVR1, but in mutant cells, it excites the receptor.

To test that possibility, the scientists developed mice that carry the FOP-causing mutation. The mice formed new bones in much the same way people with FOP do. The scientists found that if they inserted a sponge soaked in activin A into the mice, the sponge turned to bone.

If they could block activin A, the scientists reasoned, they might be able to stop the chain reaction that creates new bones. In another line of research, Regeneron scientists had developed antibodies that latched onto activin A–and only activin A. When the scientists injected these antibodies into FOP-model mice, they prevented the animals from forming any new bones. Full stop.

The fact that researchers at a company like Regeneron made this discovery is telling. Pharmaceutical companies have increasingly turned their attention to rare diseases in recent years, because, paradoxically, the rare disease market may turn out to be very profitable.

Companies are rolling out drugs with sky-high price tags. Even if they’re used by relatively few people, the companies can make a lot of money. In one demonstration of how times have changed, the rare-disease company called Baxaltra is going to be bought soon for a reported $30 billion. Whether the expensive price for rare-disease drugs are really justified, however, is becoming a matter of intense debate.

For one thing, researchers have to see if it works as well in people as it does in mice. But because people with FOP are so sensitive to injuries (even a muscle injection can trigger a new bone), regular human trials won’t work. Fortunately, Kaplan and his colleagues have discovered that they can harvest bone-generating stem cells out of baby teeth from children with FOP. So they’re now trying to replicate the activin A studies with these cells.

Setting aside the possible medical potential of this research, it drives home just how mysterious rare diseases can be. FOP might seem like it should be a simple disease to treat. After all, it’s caused by a single mutation to a single gene. But it’s actually fiendishly complex, because it disturbs an intricate web of chemical reactions that our bodies use to grow muscles and bones. The search for a cure for FOP has been going on for over a quarter of a century, and yet no one thought to consider activin A. A normal version of ACVR1 doesn’t relay activin A’s messages. And so no one even guessed that a mutant version would.

“As Alfred Hitchcock demonstrated with clarity,” Kaplan and his colleagues write, “the best way to conceal reality is to hide critical clues in broad daylight.”

The more you think about sickness and health, the trickier it gets to draw a clean line between them. We tend to think of ourselves as being prepared by nature for a good life. If we can just keep bacteria and viruses from killing us, and avoid walking into open elevator shafts, we’ll live a long, healthy life.

But we are actually the products of evolution, and evolution can’t give us perfect health. It has endowed us with powerful immune systems, thank you very much. And it has endowed us with quick reflexes that can, in some cases, keep us out of open elevator shafts. But evolution doesn’t automatically march to perfection. It stops short, leaving us with grave imperfections.

We have lots of defenses against cancer, for example, but they weaken as we get old. That’s a recipe for heartbreak in millions of families. But in the game of evolution, that’s a winning formula. Natural selection strongly favors defenses against cancer that threaten our ability to survive to adulthood and have kids. But if we die of cancer at age sixty, our kids are well on their way, carrying out genes down to the next generation.

This evolutionary perspective could change the way we think about our health in many ways. Take allergies. They affect millions of people, causing everything from hay fever to anaphylactic shock. One of the world’s leading immunologists, Ruslan Medzhitov, is convinced that allergies are actually adaptations we use to defend ourselves from noxious chemicals. As awful as allergies can get, we wouldn’t want to live without them.

I’ve written a profile of Medzhitov. It appeared today originally in Mosaic, but it’s now propagating through the Internet. You can also find it on Ars Technica, Discover, Gizmodo, Digg, and elsewhere. Check it out at the outlet of your choice. And good luck this pollen season!

In the United States—and for that matter in much of the world—the foodborne disease Salmonella is a major public health problem. Here, it causes an estimated 1 million cases every year. We tend to think of those cases, and most foodborne illness, as minor episodes of needing to stay close to the bathroom—but every year, 19,000 of them end up in the hospital and almost 400 people die. And even if they survive, people aren’t necessarily out of danger; after decades of dismissing foodborne illness as unimportant and self-limited, researchers are beginning to understand that it can have lifelong consequences.

So it’s important, as much as possible, to identify the sources of Salmonella infection, and to alert people to the ways in which they can protect themselves.

And that’s why the Centers for Disease Control and Prevention, the CDC, is worried about those fluffball Easter chicks that might be appearing in households this weekend, as well as the juvenile poultry that backyard farmers and urban locavores may begin buying as the weather warms.

As I mentioned in my intro post yesterday, I also am writing for National Geographic‘s food site, The Plate, and I have a new post up there about the under-appreciated danger posed by live baby poultry. Whether you are buying them for immediate adorableness on top of an Easter basket, or eventual eggs or meat in a small-scale coop, most of us find baby chicks irresistible, in the hard-wired way that makes us melt before kittens and babies too. So we cradle them, and cuddle them, and smooch them on top of the head. But we forget that, just like babies of every other species, they are poop machines. And Salmonella travels in poop.

This isn’t an argument against buying baby poultry, especially not if you’re doing it for small-scale egg or meat production. (Animal welfare organizations urge not buying baby animals just for Easter, because of the likelihood they will be dumped.)

But it is a plea on behalf of something I’m probably going to be saying a lot as we go forward: Don’t forget to wash your hands.

In this Sunday’s issue of the New York Times Magazine, I have a feature about clashing visions of the genome. Is it overwhelmingly made up of “junk”–pieces of DNA that provide us with no useful function–or is it rife with functional pieces that we have yet to understand? Or is the reality of the genome a confusing mixture of the two?

To research this story, I shed some blood so that I could compare my genome to that of an onion. This print-out, annotated by T. Ryan Gregory, shows that an onion has five times more DNA in its genome than mine. I also spent time in the lab of John Rinn at Harvard, where scientists are discovering hints that our genome encodes exotic molecules that may be essential for our well-being. And I talked to a range of scientists about the challenges of understanding what any given piece of DNA is “for,” and what sort of assumptions one should bring to the challenge. Finally, I dug deep into the history of this question, which has roots reaching all the way back to Darwin. Check it out.

Courtesy of T. Ryan Gregory

P.S. This is an incredibly rich topic, and I welcome readers to discuss it (especially the stuff I didn’t have room to get to in my feature) in the comment thread below. I’ll also post some interesting papers here, too.

In November, National Geographic put a ladybug and a wasp on its cover. They made for a sinister pair. The wasp, a species called Dinocampus coccinellae, lays an egg inside the ladybug Coleomegilla maculata. After the egg hatches, the wasp larva develops inside the ladybug, feeding on its internal juices. When the wasp ready to develop into an adult, it crawls out of its still-living host and weaves a cocoon around itself.

As I wrote in the article that accompanied that photograph, the ladybug then does something remarkable: it becomes a bodyguard. It hunches over the wasp and defends it against predators and other species of parasitic wasps that would try to lay their eggs inside the cocoon. Only after the adult wasp emerges from its cocoon does the bodyguard ladybug move again. It either recovers, or dies from the damage of growing another creature inside of it.

How parasites turn their hosts into zombie slaves is a tough question for scientists to answer. In some cases, researchers have found evidence suggesting that the parasites release brain-controlling chemicals. But the wasp uses another strategy: there’s a parasite within this parasite.

In the Proceedings of the Royal Society, a team of French and Canadian researchers now lay out the evidence for this strange state of affairs. As they studied this manipulation, they reasoned that the best place to look for clues was inside the heads of parasitized ladybugs. They discovered that the brains of these hosts were loaded with viruses. When the scientists sequenced the genes of the virus, they found it was a new species, which they dubbed D. coccinellae Paralysis Virus, or DcPV for short.

The scientists found DcPV in the wasps as well–but not in their brains. In female adult wasps, the virus grows in the tissues around their eggs. Once a wasp egg hatches inside a ladybug, the virus starts replicating inside it, too. The larva then passes on the virus to its host, and the ladybug develops an infection as well.

DcPV causes no apparent harm to the wasps, but the ladybug is not so lucky. The virus makes its way into the ladybug’s head, where it attacks brain cells and produces new viruses in pockets inside the cells. Many brain cells die off during the infection.

The researchers hypothesize that the virus is responsible for the change in the ladybug’s behavior. To get the ladybug to guard the wasp, the virus may partially paralyze its host, so that it becomes frozen over the parasite. Because the paralysis isn’t complete, the ladybug can still lash out against predators. But these may just be wild spasms in response to any stimulus. The bodyguard effect may grow even stronger as the infection robs the ladybug of the signals from its eyes and antennae. Closed off the world, its sole purpose becomes protecting its parasite.

The fate of a parasitized ladybug–to die or to walk away–may depend on how it handles a DcPV infection. In some cases, the virus may be fatal–possibly by triggering a massive immune response that kills not just the virus but the ladybug itself. In other cases, the ladybug’s immune system may eventually be able to clear the virus out of its system, letting its nervous system heal.

In either case, the bodyguard paralysis lasts long enough to protect the wasp while it develops into an adult. Whether the ladybug lives or dies doesn’t matter to the wasp–or to the virus. The new wasp carries a fresh supply of DcPV. If it’s a female, it will be able to use the virus to infect both its own young, and its ladybug slave.

In recent years, scientists have developed a deepening appreciation for the importance of our microbiome–of the bacteria and viruses that make our bodies their home. While some microbes invade our bodies, others reside inside of us and help keep us healthy. Parasitic animals have microbiomes of their own, and this new study suggests that they can use them for suitably sinister ends.

(For more information on the sophisticated tricks of parasites, see my book Parasite Rex.)

The Steller’s sea cow is gone. This mega-manatee swam the North Pacific for millions of years, and then in the 1700s humans hunted them to extinction. Today on the front page of the New York Times, I write about a warning from a team of scientists that if we keep on doing what we’re doing now–industrializing the ocean and pouring carbon dioxide into the atmosphere in greater and greater amounts–a lot of other marine animal species will go the way of the Steller’s sea cow.

Yet this story is actually a fairly hopeful one. The scientists compared the pace of extinctions at sea to those on land and found that the oceans are basically where the land was in 1800–with relatively few extinctions yet, on the verge of massive changes to the habitat that could wreak much bigger havoc. The oceans still have a capacity to recover, if we choose to let them.

It’s hard to strike that balance, but it’s important. By coincidence, a group of marine biologists has just published a provocative opinion piece calling for more skepticism about “ocean calamities”–the claim that the oceans are getting hit with some global shock of one sort or another. (You can read the piece in Bioscience for free.) They complain that too often scientists see a small-scale change in one region of the ocean and blow it up to a global catastrophe. The scientists pick apart some of these cases, such as the belief that jellyfish are taking over the planet. The strongest evidence for their rise turned out to be a natural increase of one population of jellyfish that is part of a natural cycle.

That doesn’t mean that thee are no ocean calamities. The scientists see strong evidence for devastation from overfishing, for example. And that doesn’t mean that dangers that don’t seem to have had big impacts yet won’t have them in the future (see ocean acidification). But leaping to the apocalypse based on limited or ambiguous evidence is bad science and bad policy, the scientists argue:

We conclude that a robust audit of ocean calamities, probing into each of them much deeper than the few examples provided here, is imperative to weeding out the equivocal or unsupported calamities, which will confer hope to society that the oceans may not be entirely in a state of near collapse and which will provide confidence that the efforts by managers and policymakers targeting the most pressing issues may still deliver a healthier ocean for the future.

I wanted to check in with the authors of the Bioscience piece about the new study I wrote about for the Times. If they thought this new study was an egregious case of calamity-mongering, I needed to know that, and I would make it clear in my piece.

But that’s not what I found. When I spoke to Robinson Fulweiler, a marine biologist at Boston University, she said, “I was really excited to read their paper, and I actually felt good about their conclusions.” She thought the scientists did a good job of gauging what’s happened to the oceans so far, the risks they face in the future, and–importantly–the steps that we can take, armed with our knowledge of the situation.

When we’re contending with our effects on the planet, it may be tempting to go limp and say we’re all doomed, or to wave it off as some huge delusion. But the reality of the oceans calls for a different response altogether.

Human sexuality is obviously complicated. But it’s a mistake to think that, if you could somehow strip away human culture, sex would get simple. Even if you could find the simplest animal out there with a sex life, you wouldn’t find that imaginary simplicity.

This week I’ve written an essay on just such an animal, the worm Caenorhabditis elegans. With only a thousand cells in its entire body, the worm is unquestionably simple But it’s also arguably the best-studied animal on the planet. And yet its sex life–featuring self-fertilizing hermaphrodites with some males on the side–remains bizarrely mysterious.

You’d be forgiven for calling FTO the “fat gene.” There are two variants of the gene, and in study after study, one of those variants, known as rs993609, is associated with more weight, as well as a much higher risk of obesity. The comparison holds up in different countries, and in different ethnic groups. The link is so clear that it might seem like saying FTO can make you fat is as true as saying two plus two equals four.

Now try to imagine discovering that before World War II two plus two equaled zero.

That’s the gist of a new study on FTO’s effects over time. As I explain in my new “Matter” column for the New York Times, scientists have looked at the link between FTO and body-mass index in a long-term study of thousands of people over many decades. They found that people born before 1942 show no link. None. The link is strong in people born afterwards, and gets stronger with time.

I find this study interesting because it provides a twist on the old debate about nature versus nurture. Take two people with identical genes and put them in different environments, and some of their genes may respond in different ways. That’s long been a good counterargument against genetic hyper-determinism. Here’s a case where the entire environment–the world in which we live, work, and eat–has changed. As a result, a gene that would have gone overlooked if scientists looked for it a couple generations ago now leaps out as a clear factor in one of the world’s most pressing medical problems.

It’s possible that other genes will show patterns of their own over time. Putting a time axis on how genes affect our health may make studying the matter far more challenging–as well as using that information to guide medicine. What proves true now may not be true a few years from now.

PS– There’s a fascinating side-story about FTO that I didn’t have space to get into, which University of Chicago geneticist Vincent Lynch raised on Twitter. Ever since FTO’s effect was discovered in 2007, scientists have been puzzling over how that effect comes about. They’ve discovered that the FTO protein does all sorts of interesting things, including affecting the brain biochemistry involved in appetite. But a study that came out in March suggests the risk variant may have nothing to do with the FTO protein at all.

“Wha….?” you say? Well, here’s the thing. A gene like FTO is made up of two different kinds of pieces of DNA, called introns and exons. Cells make FTO proteins by only reading the exons of the FTO gene, essentially ignoring the introns. Packing genes with unread DNA may not sound smart, but evolution doesn’t build life the way you might.

It turns out that the rs993609 mutation sits in an intron in the FTO gene. So it doesn’t appear to change the FTO protein. Instead, scientists suspect that the rs993609 mutation sits in a little stretch of DNA in that intron, called an enhancer. They speculate that this enhancer can somehow coax our cells to make copies of another gene that lies elsewhere in our DNA. The rs993609 mutation changes how the enhancer acts on that other gene.

So rs993609 is “in” the FTO gene–in a geographical sense–and yet the FTO gene itself may not make post-war folks fat.

This molecular mystery doesn’t affect the patterns in the new study I wrote about in my column. But it will be important to understanding the biology of obesity. And it serves as a good lesson in how tricky it can be to talk about genes.

Thanks to everyone for sharing a year of science with me over the course of 2014. It was a year of frantic writing, as I tried (and failed) to keep up with all of the new research that expanded my appreciation of the natural world. In addition to blogging here, I wrote my weekly “Matter” columns for the New York Times, published a few longer pieces, and spent time in Second Edition World, revising a couple of my books. (Details to come in a few months.)

Looking over the year, I put together a list of the pieces I was most fond of (plus some radio work). If you’re looking for some reading (or listening) to fill the languorous spaces between gift-opening and holiday-meal-snarfing, check these out…

One of the biggest surprises to come out of microbiology in recent years is that bacteria have a social life. Rather than existing as lonely, autonomous creatures, bacteria live in communities, in which they cooperate, compete, and communicate. In the January issue of Scientific American, I have a feature about how some scientists are trying to translate their growing understanding of the social life of bacteria into a new kind of medicine. By preventing microbes from cooperating, we may be able to bring infections to a halt. Better yet, this kind of antisocial medicine may even be able to avoid–or at least slow down–the evolution of drug resistance in bacteria.

For many paralyzed people, their problem is a communication gap. They can generate the signals in their brain require to control their muscles–to walk, to wash dishes, to weed a garden. But damage to their nervous system prevents those signals from reaching their destination.

Last year, in a feature I wrote for National Geographic about the brain, I recounted the work of scientists and engineers who are trying to bridge that gap. Their dream is to create a technology that reads signals from people’s brains and uses them to control machines. The machines might be robot arms that people could use to feed themselves, or computers to compose emails, or perhaps even exoskeletons that could enable people to walk.

Scientists have been investigating these brain-machine interfaces for decades, and in recent years they’ve made some impressive advances–some of which I described in my story. But it would be wrong to giddily declare that scientists have reached their goal. You need only look at this picture below to get a sense of how far we are from science-fiction dreams.

UPMC

This woman, Jan Scheuermann, is at the forefront of brain-machine interface research. She volunteered to have an electrodes injected into the surface of her brain. Researchers at the University of Pittsburgh connected the electrodes to pedestals on top of her scalp. Cables can be attached to the pedestals; they connect to a computer and a power source.

Scheuermann and the scientists worked together to train the computer to recognize signals from her brain and use them to control a robot arm. In December 2012, Scheuermann made news by controlling the robot arm so well she could feed herself a bar of chocolate.

But this system was hardly ready for prime time. The electrode apparatus has to pass through a hole in a patient’s skull, creating the risk of infection. The cables tether the patient to bulky machines, which would make the whole system cumbersome rather than liberating.

In addition, the robot arm had plenty of room for improvement. It had seven degrees of freedom. Scheuermann could control its shoulder, elbow, and wrist joints. The hand, however, could only open and close. So Scheuermann had the same kind of dexterity as if she wore a mitten.

A 1958 pacemaker–wired to a cart of machines. Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232561/

None of this was any reason to dismiss brain-machine interfaces as having reached a dead end. The history of pacemakers started out in much the same place. Today, people can walk around with pacemakers implanted in their chests without anyone around them having the slightest awareness that a device is regulating their heartbeat. Sixty years ago, however, the first pacemakers were enormous, cumbersome affairs. Implanted electrodes were tethered to wires that ran to big machines. Patients either had to lay next to the machines or trundle them around on a cart. The pacemakers were also relatively simple, delivering fixed patterns of electricity to the heart. Too often, they failed to keep the heart working.

In the 1960s, pacemakers became portable and battery-powered. They still needed external wires, but the wires now ran to a small box that a patient could carry on a belt. Finally, pacemakers disappeared into the body completely. In 2009, doctors began implanting pacemakers that not only had their own power supply but could also communicate medical information to doctors with a Wi-Fi connection to the Internet. Pacemakers also deliver more sophisticated signals to the heart, using algorithms to adjust their rhythms. If someone looked at the ungainly state of pacemakers in 1960 and declared them hopeless, they would have been profoundly wrong.

Two new studies are pushing brain-machine interfaces forward in the same way.

The first study advances the electrode end of the interface. A team of scientists led by Arto Nurmikko of Brown University developed an implant that requires no wires. The implant can pick up signals from 100 different electrodes. It contains microelectronics that can turn these signals into a Wi-Fi transmission broadcast at a rate of 200 Mb per second. The researchers implanted the device in monkeys and found that they could pick up signals from five yards away with a quality on par with signals delivered by cables. The monkeys went about their business freely, and the scientists could pick out signals they used to walk on a treadmill. When the monkeys fell asleep, the scientists could detect shifts in their brain waves. The whole apparatus runs for over two day straight on a double AA battery.

For now, this device will probably be most useful to researchers who study the behavior of animals. But Nurmikko and his colleagues are also learning lessons for the next generation of brain-machine interfaces for people. In another promising line of research, they have designed a prototype of a fully implantable device. The electrodes go in the brain, while the power source and transmitter sit atop the skull, below the scalp. In the future, scientists may be able to make new devices that take advantage of both studies–implants that can be sealed in the head, transmit a lot of data wirelessly, run efficiently on a long-lasting battery, and not heat up the way electronics sometimes do.

Meanwhile, at the other end of the interface, Scheuermann has been testing out a new and improved robot arm. The Pittsburgh team programmed four different positions that the hand could take, such as pinching the index and thumb together. The researchers had no idea if all those extra degrees of freedom would be too much for their interface to handle. Could it pick out signals in Scheuermann’s brain that were meaningful enough to make full use of the arm’s range of motion?

To train Scheuermann, the scientists had her start her practice on a virtual robot arm, which she used to grab virtual objects on a computer screen. The computer system learned how to recognize certain patterns of neuron signals as commands to change the shape of the robot hand. At the same time, Scheuermann’s own brain became more adept at controlling the robot arm, producing stronger signals. Finally, the scientists had Scheuermann try to pick up a number of different objects. Here’s a sampling of her successes:

Scheuermann, as the scientists had hoped, learned how to manage her new arm. It wasn’t a perfect education. Scheuermann sometimes failed to grab objects, and the scientists never managed to record a success on certain tasks, such as pouring water from one glass into another.

Still, the results were encouraging–and sometimes intriguing. The scientists found some groups of neurons that would fire together in distinctive patterns as Scheuermann moved the arm through all ten dimensions. In other words, these neurons weren’t limited to just bending the elbow or pinching a thumb. In the future, it may be possible to harness these flexible signals to make the arms even more proficient, and to fill the communication gap even more.

This week I wrote my New York Times column about one of those remarkable studies that makes you realize how little we understand about the natural world. Ken Catania, a biologist at Vanderbilt University, performed some elegantly simple experiments that revealed that electric eels use electricity as a taser and as a remote control for their prey.

To read mostly straight-text accounts of the research, you can read my column, as well as fellow Phenom Ed Yong’s blog post. But the video that Catania filmed as part of his research is so interesting I thought offer a moving-pictures recap here.

Here’s what it’s like when an eel goes after a fish. The eel’s pulses of electricity are converted to sound. Basically, there’s an electric blast, a lunge, and it’s all over for the little fish.

But when Catania slowed down his video (he films it at 1000 frames a second), he could see that right after the eel starts sending out pulses, the fish just froze. Here are a couple examples. The red frames show when the eel is discharging electricity. The blast contracts all the fish’s muscles at once, causing the animal to freeze. It’s a natural taser.

Finally, here’s a movie that shows how the eel can flush out hidden prey. The fish here has its brain removed, and it’s tucked away in a walled-off recess in the eel’s tank. The barrier is made of agar, which allows electricity and waves to pass through.

The eel comes up, giving off short paired pulses of electricity. These pulses are like probes. Instead of immobilizing the fish, the pulses make the fish twitch. The waves set off by the twitch reveal its hiding place, and the eel comes in for a taser attack.

Family life is fascinating–whether the family involved is made up of humans, monkeys, or hippos. Recently I’ve been exploring the complexities of mammal family life, and I’ve been thinking about what this research can and cannot tell us about our own experiences in families.

Last week in the New York Times, I wrote my column about some intriguing research on what happens when monkey mothers nurse their babies. Their milk doesn’t just deliver nutrients. It also has messages–different levels of hormones–that influence how babies develop, both physically and psychologically.

It may sound strange, but the “why” of infanticide has a lot in common with the “why” of nursing’s effects on babies. In both cases, scientists have found evidence that these are adaptive responses. In the case of nursing, the babies appear to be reading the messages in their milk to judge the condition of their mother. They’re then adjusting their development to make the best use of her resources. In the case of infanticide, males that compete with other males to be with females can get more of an opportunity to have babies of their own by killing unrelated babies first.

Both stories are fascinating, and not just for their immediate results. We can’t help but wonder what scientific research of other mammals may tell us about ourselves. Yet the insights are not straightforward, and so we have to be on our guard not to draw simplistic conclusions.

We don’t yet know how much of an influence hormones in milk have on human development, for example. Monkeys and humans both nurse, but they nurse in very different ways (human mothers don’t keep their babies nursing constantly, for example). And human babies are influenced by many other factors as they develop.

As for mammal infanticide, it may be tempting to see it as an explanation for human child abuse. But you can’t draw a simple parallel between, say, the death of a human child in a chaotic home where there’s been lots of drug abuse and the death of a baby monkey that’s been systematically stalked for days by an adult male.

Nor do these stories give us easy answers about what is right or wrong in human family life. To try to make that leap is to commit a moralistic fallacy. I’ve had a lot of experience watching people make that fallacy. That’s one of the hazards of reporting on evolution.

I first wrote about infanticide 18 years ago. I was working at Discover, and I had taken a trip to Sumatra not long before, where I had spent some time with scientists at a forest reserve. Some of them were following monkeys, observing their family life. They told me how males sometimes killed babies. There were no killings when I was there, which isn’t surprising given that they happen quickly and relatively rarely. But even as I watched the monkeys leap through the high canopy, busy with their own complicated social lives, I kept wondering about why they would turn homicidal.

When I got back home, I spoke to Sarah Hrdy, an anthropologist who developed the argument that infanticide is part of a reproductive strategy in the 1970s. I talked to her critics, and I also talked to scientists who found evidence for infanticide in other species. You can read the feature I ended up putting together here. (Here’s a site where Hrdy keeps a lot of papers.)

Shortly after the article came out, the creationists came after me. Specifically, the president of the Institute of Creation Research at the time, John D. Morris. He published a piece called, “Will Infanticide Follow Abortion As Acceptable Behavior?”

He ended it this way:

The discussion reviewed her [Hrdy’s] theories and others who followed, but the most chilling aspect was the possible use of this animal behavior as a model for human behavior. The article’s author, Dr. Carl Zimmer, stopped short of advocating human infanticide, but clearly the issue was raised and not discarded. Those who today practice infanticide were discussed without condemnation. A comparison to the disparity in frequency of child-killing between biological fathers and step-fathers was made. Nowhere was the practice of infanticide condemned, and, of course, no mention was made of it as a sin.

The article did speculate on the various reasons why langurs (and other animals) choose to kill their young, and comparisons were made to human situations. The reader is left to shudder at the thought of the possibilities, but be numbed to its consequences, by greater familiarity with it.

One only has to look at Hitler’s Germany to recognize similarities. Atrocities escalated until unthinkable things were attempted. It is my conviction that the trends in this country are the same. A wholesale turnover of politicians, media elite, and education theorists would help to stem the tide. The groundwork has already been laid, the damage may have already been done. We will soon reap even more awful fruits of evolutionary thinking, unless we go “Back to Genesis.”

Morris was wrong in all sorts of ways (beginning with the fact that I’m not “Dr.” Zimmer). But his screed was valuable as an example of how easily people can–intentionally or not–make a fallacious leap from nature’s “is” to human “oughts.” In order to make our own moral judgments–about breast-feeding, about protecting children from abuse–we need to understand how evolution has shaped us. That’s no simple task, and when it comes to judging the right thing to do for children, it’s just the beginning.

A couple viruses are waving hello to the United States right now. Flu season is about to kick off, while people have been diagnosed with Ebola not just in Texas, but in New York. But there are some important differences between the two viruses that I explore in an article in today’s New York Times. Most importantly: there’s no evidence that Ebola spreads through the air like the flu.

I’ve written the cover story for the new November issue of National Geographicabout the biology of parasite manipulation. I’ve been obsessed by this subject for a long time. (In my book Parasite Rex I wrote a chapter on this bizarre slice of reality). So it’s a huge delight to help give these mind-controllers the Nat Geo treatment: gorgeous pictures. When I wrote Parasite Rex, I gathered up what photos I could find, but none of them did the parasites justice. Anand Varma has journeyed to a number of countries to find the creepiest examples of this surprisingly common (and medical useful) phenomenon.

Anand and I will be speaking at the National Geographic Society in Washington DC about the story and photos on October 29. Please join us. Details are here.

Who We Are

Phenomena is a gathering of spirited science writers who take delight in the new, the strange, the beautiful and awe-inspiring details of our world. Phenomena is hosted by National Geographic magazine, which invites you to join the conversation. Follow on Twitter at @natgeoscience.

Ed Yong is an award-winning British science writer. Not Exactly Rocket Science is his hub for talking about the awe-inspiring, beautiful and quirky world of science to as many people as possible.
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